Inhibition of ultraviolet C irradiation-induced AP-1 activity by aspirin is through inhibition of JNKs but not erks or P38 MAP kinase.
The exposure of mammalian cells to ultraviolet (UV) irradiation leads to the activation of transcription factors, such as AP-1 and NFkB. We demonstrate that aspirin, a promising cancer chemopreventative agent, inhibited UVC-induced AP-1 activity in JB6 cells. In JB6 cells, UVC stimulated Erks, JNKs and P38 kinase activities; aspirin only inhibited activation of JNKs, but not the other MAP kinases. Since the transcription factor AP-1 is important for the process of tumor promotion, the inhibitory effect of aspirin on AP-1 activation suggests that it can be used as a chemopreventative agent against skin cancer.
Ma
W Y
WY
The Hormel Institute, University of Minnesota, Austin, Minnesota 55912, USA.
Huang
C
C
Dong
Z
Z
D000818:Animals; D016588:Anticarcinogenic Agents / Q000494:pharmacology; D001241:Aspirin / Q000494:pharmacology*; D017871:Calcium-Calmodulin-Dependent Protein Kinases / Q000037:antagonists & inhibitors / Q000378:metabolism*; D002460:Cell Line; D004305:Dose-Response Relationship, Drug; D017930:Genes, Reporter; D048031:JNK Mitogen-Activated Protein Kinases; D051379:Mice; D020928:Mitogen-Activated Protein Kinases; D011993:Recombinant Fusion Proteins / Q000096:biosynthesis / Q000378:metabolism; D018808:Transcription Factor AP-1 / Q000187:drug effects / Q000378:metabolism* / Q000528:radiation effects; D014162:Transfection; D014466:Ultraviolet Rays; D048051:p38 Mitogen-Activated Protein Kinases
D016588:Anticarcinogenic Agents; D011993:Recombinant Fusion Proteins; D018808:Transcription Factor AP-1; D017871:Calcium-Calmodulin-Dependent Protein Kinases; D048031:JNK Mitogen-Activated Protein Kinases; D020928:Mitogen-Activated Protein Kinases; D048051:p38 Mitogen-Activated Protein Kinases; D001241:Aspirin